Cancer stem cell theories offers the prospect that various types of cancer spawn from characteristic stem-cell-like initial populations. Cancer exists because random mutations that occur in our cells as a result of damage and age will eventually produce one of these prolific and damaging cell types, possibly by damaging an existing adult stem cell, or possibly by radically mutating a normal somatic cell. Cancer stem cells are hard to eradicate completely through old-style chemotherapy, radiotherapy, or surgery, which is why cancers tend to recur - all it takes is one remaining errant stem cell to rebuild the cancer anew. But the nature of cancer stem cells also means that they are the weak link: destroy them and the cancer cannot survive. Fortunately, identifying and safely destroying specific cell types based on their biochemical differences is a core focus for biotechnology research these days. This is one of the reasons I am confident that my generation will not suffer greatly from cancer in later life: the cancer-killing therapies of three decades from now will be very safe, very effective, and very cheap.
On this topic, I noticed a few recent articles on cancer stem cell research and development today, and thought I would share.
"Think about cancer as a disease of stem cells," said study coauthor Owen Witte, a Howard Hughes Medical Institute investigator at the University of California, Los Angeles. Mutations in these cells can cause "normal stem cells to lose their regularized behavior and instead turn into an incipient cancer," he said. Like many other tissues in the body, prostate tissue is made up of several different kinds of cells, including a class called basal stem cells. Normally these cells divide to replenish prostate tissue, but sometimes they become cancerous. Instead of producing normal cells, these stem cells lead to tumors.
"Targeting cancer stem cells, rather than cancer cells, is a completely new strategy for treating cancer," said Dr. Stephen Wong, director of the Center for Bioengineering and Informatics at The Methodist Hospital Research Institute and principal investigator for the grant study. "By attacking the cancer stem cell, we hope to eliminate cancer’s ability to grow, recur or metastasize."
Recent studies have increased our understanding of cancer by elucidating some of the differences that exist between tumor cells among patients and even between distinct subsets of tumor cells within the same patient. Evidence suggests there are subgroups of cells - called cancer stem cells or tumor initiating cells - within tumors that are harder to kill with current therapies than other cells within these tumors. Cancer stem cells may in fact be more important to destroy than non-cancer stem cells because they may be responsible for metastasis and for tumor recurrence after therapy. Identifying therapies which specifically target cancer stem cells therefore hold great promise for effective and lasting treatment.
The original paper for that last item makes for interesting reading. You should take a look. But of course things are never as simple as we'd like them to be. Cancer stem cells may not be at the base of all cancers, and there are strong arguments that might lead us to expect this to be the case. This final article from earlier in the month delves into some of these complications.
The stochastic, or clonal evolution, model dictates that, "despite the heterogeneity (in cancer), cells of many different phenotypes are capable of proliferating extensively and forming new tumors," Dr. Morrison summarized. The cancer stem cell model, in contrast, says that "cancer stem cells are uniquely capable of proliferating extensively and forming new tumors, and that they go through an aberrant process of differentiation giving rise to phenotypically diverse cancer cells with a limited capacity to divide." Which of these two theories is correct seems to depend upon the type of cancer.